RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
CD15(+) 骨髓来源细胞是产生 ARG1 的结直肠癌细胞中免疫应答的调节因子
英文原题：CD15(+) Bone Marrow-derived Cells Are Regulators of Immune Response in ARG1-producing Colorectal Cancer Cells.
查看英文原题
CD15(+) Bone Marrow-derived Cells Are Regulators of Immune Response in ARG1-producing Colorectal Cancer Cells.
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研究概要
肿瘤浸润性 CD15+细胞，其中大多数表现为多形核特征，是导致人结直肠癌中 ARG1 依赖性 T 细胞功能障碍的原因。
研究思路结论见上方概要
背景
骨髓来源细胞通过精氨酸酶1（ARG1）依赖性代谢调控TIL（肿瘤浸润淋巴细胞）的抗肿瘤功能。本研究探讨哪种产生ARG1的细胞谱系负责TIL的抑制功能。
方法
在人类结直肠癌标本中，对CD11b、CD163、CD68和CD15进行了多重免疫组织化学检测，同时评估了ARG1表达和CD3+ TIL浸润情况。
结果
分层生存分析显示，大量CD3 + TIL是高水平ARG1 + 浸润亚组以及低水平ARG1 - CD15 + 浸润亚组中的有利预后因素。计算ARG1 + /ARG1 - 比值表明，CD3 + TIL浸润在CD15 + 细胞低ARG1 + /ARG1 - 比值亚组中具有预后意义，而其他谱系则相反。
展开英文摘要原文
MATERIALS AND METHODS
Multiplexed immunohistochemistry was performed for CD11b, CD163, CD68, and CD15, together with ARG1 expression and CD3 + TIL infiltration estimation in human colorectal cancer specimens.
RESULTS
Stratified survival analyses demonstrated that a large number of CD3 + TILs is a favorable prognostic factor in subgroups with a high level of ARG1 + infiltration and in the subgroup with a low level of ARG1 - CD15 + infiltration. Calculation of the ARG1 + /ARG1 - ratio demonstrated that CD3 + TIL infiltration was prognostic in the subgroup with a low ARG1 + /ARG1 - ratio for CD15 + cells, contrary to other lineages.
CONCLUSION
Tumor infiltrating CD15 + cells, the majority of which show polymorphonuclear features, are responsible for the ARG1-dependent T-cell dysfunction in human colorectal cancer.
论文信息
- 作者
- Miyoshi K、Sato E、Katsumata K、Fukushima G、Udo R、Nishimura E、Tago T、Kasahara K
- 第一作者单位
- Department of Gastrointestinal and Pediatric Surgery, Institute of Medical Science, Tokyo Medical University, Tokyo, Japan.Japan
- 通讯作者单位
- Department of Pathology, Institute of Medical Science, Tokyo Medical University, Tokyo, Japan sato-e@tokyo-med.ac.jp.Japan
- 期刊
- Anticancer research2022 Jan
- 原文标识
- PubMed 34969756 · DOI 10.21873/anticanres.15504